Cannabinoid science glossary

2-AG (2-arachidonoylglycerol) is an endocannabinoid, one of the signalling lipids the body makes for itself, and generally the most abundant of them. Cells build it from membrane fats at the moment they need it. It activates both the CB1 and CB2 cannabinoid receptors, and dedicated enzymes clear it away soon after.

Why it matters: Long before anyone bottled a hemp extract, 2-AG and anandamide were running the endocannabinoid system as its two main messengers. The receptors a CBG or THC product reaches belong to machinery the body already operates with molecules of its own.

Related: endocannabinoid, anandamide, CB1 receptor, CB2 receptor, Endocannabinoid system (ECS)

The 5-HT1A receptor is a G-protein-coupled serotonin receptor involved in mood and anxiety signalling. It belongs to the serotonin system, yet several cannabinoids reach it, and a compound can either activate it (an agonist) or block it (an antagonist).

Why it matters: Here CBG and CBD pull in opposite directions. In laboratory (in vitro) studies CBG is a 5-HT1A antagonist (Cascio 2010; Demonstrated · in vitro), while CBD acts as an agonist at the same receptor. Evidence gathered on one cannabinoid cannot be assumed to carry over to another: CBD's research describes CBD, and CBG has to earn its own.

Related: agonist, antagonist, Cannabinoid receptor, CBG, cbd

Grade: Established (receptor identity) · Demonstrated · in vitro (CBG's antagonism)

An agonist is a molecule that binds a receptor and activates it, producing the receptor's signal: the key that fits the lock and turns it. A full agonist drives the receptor to its maximum response; a partial agonist stops short of that. The body's own endocannabinoids are agonists at cannabinoid receptors.

Why it matters: Whether a cannabinoid is an agonist or an antagonist at a given receptor often decides which way its effect runs. THC is intoxicating because it activates (is an agonist at) the CB1 receptor.

Related: antagonist, Partial agonist, Inverse agonist, Cannabinoid receptor

Anandamide (AEA, short for arachidonoylethanolamide) is an endocannabinoid that activates the CB1 receptor, and CB2 more weakly. Like 2-AG, it is made on demand from membrane fats and broken down quickly. The name comes from the Sanskrit ananda, "bliss."

Why it matters: Anandamide settles where the endocannabinoid system comes from: native human biology, borrowed from nowhere. Plant cannabinoids are the visitors, acting on receptors that exist to serve molecules the body already makes.

Related: 2-AG (2-arachidonoylglycerol), endocannabinoid, CB1 receptor, Endocannabinoid system (ECS)

An antagonist is a molecule that binds a receptor without activating it, and so blocks or dampens the receptor's normal signalling. In the lock analogy the key fits and jams, and while it sits there every other key stays out. Its whole effect comes from occupying the receptor.

Why it matters: Much of the gap between CBG and THC comes down to this word. In laboratory studies CBG acts as an antagonist at several targets, including the CB1 and 5-HT1A receptors (Cascio 2010; Demonstrated · in vitro).

Related: agonist, Inverse agonist, CB1 receptor, 5-HT1A (serotonin) receptor, CBG

The α2-adrenoceptor is a G-protein-coupled receptor for noradrenaline (norepinephrine), part of the adrenergic system that helps regulate blood pressure, heart rate and alertness. Switch it on with an agonist and noradrenaline release tends to fall. It sits outside the classic cannabinoid receptors, yet some cannabinoids act on it.

Why it matters: Few targets say more about CBG. In laboratory (in vitro / ex vivo) studies, CBG behaves as a potent agonist at the α2-adrenoceptor (Cascio 2010; Demonstrated · in vitro), one of its most distinctive characterised actions. Blood-pressure caution: because this receptor helps regulate blood pressure, anyone taking cardiovascular or blood-pressure medication, or with a cardiovascular condition, should consult a clinician before using CBG. (not medical advice)

Related: agonist, CBG, Receptor affinity, Endocannabinoid system (ECS)

Grade: Established (receptor identity) · Demonstrated · in vitro (CBG's agonism)

Bioavailability is the fraction of a dose that reaches the bloodstream in active form, and how quickly it gets there. For cannabinoids taken by mouth it is generally low and variable. They are lipophilic and dissolve poorly in water, and a swallowed dose has to pass through the gut and liver before it reaches general circulation. Product format (sublingual, inhaled, oil-based or emulsified) and whether the product goes down with food noticeably change how much is absorbed. Established (general cannabinoid pharmacokinetics; specific figures vary widely and are left out here).

Why it matters. The milligrams printed on the label and the milligrams that reach the blood are two different numbers. For a formulator the delivery format is part of the dose, and a dosing claim that ignores absorption is built on sand.

Related: first-pass metabolism · solubility · logP / lipophilicity · CYP450 enzymes

Biosynthesis is the chain of enzyme-driven steps by which a living organism assembles a molecule. In cannabis the chain starts when two small building blocks, olivetolic acid and geranyl pyrophosphate, are joined into CBGA, the central acid. Synthases, the branch enzymes, then turn CBGA into THCA, CBDA and CBCA. Each of those acids stays an acid until heat drives decarboxylation and yields the familiar neutral cannabinoid. Established

Why it matters. The pathway is the backbone of the cannabinoid family tree and the reason CBGA earned its "mother" nickname. It also draws the line between what the plant produces (acids) and what people usually consume (neutral forms).

Related: CBGA (cannabigerolic acid) · synthase enzyme · cannabinoid acid · decarboxylation

A cannabinoid is any compound that acts on the body's endocannabinoid signalling system, shares the characteristic cannabinoid chemical scaffold, or both. The family covers plant-made (phyto-) cannabinoids such as CBG, CBD and THC, the body's own (endo-) cannabinoids, and lab-made (synthetic) ones. Established

Why it matters. Everything in this Atlas sits under the umbrella. Used precisely, the word stops "cannabinoid" being read as a synonym for THC, or for "intoxicating."

Related: phytocannabinoid vs endocannabinoid · cannabinoid acid · varin cannabinoid

A cannabinoid acid is the raw form the plant makes, still carrying a carboxylic-acid (–COOH) group: the "A" in CBGA, CBDA, THCA, CBCA and in the varin acids THCVA, CBGVA and CBDVA. Most cannabinoids in the living plant exist as acids. In that form they are non-intoxicating, and heat (decarboxylation) converts them to their familiar neutral counterparts. Established

Why it matters. The acids explain why raw cannabis stays non-intoxicating until someone heats it, and why a lab report or label may list "THCA" or "CBDA." Acid versus neutral is basic chemistry, whatever the marketing makes of it.

Related: decarboxylation · CBGA (cannabigerolic acid) · biosynthesis · synthase enzyme

A cannabinoid receptor is a protein on a cell that cannabinoids bind to, changing the signals the cell sends. The best characterised are CB1 and CB2, both part of the endocannabinoid system and normally switched on by the body's own endocannabinoids. Cannabinoids also act at a wider cast of receptors and ion channels beyond that pair.

Why it matters: In casual use the term shrinks to CB1 and CB2, yet many of the cannabinoid actions measured in the lab happen at other targets entirely. Cannabinoid pharmacology turns out more varied, and far less interchangeable, than the shorthand suggests.

Related: CB1 receptor, CB2 receptor, Endocannabinoid system (ECS), trpv1, 5-HT1A (serotonin) receptor

Catalogue in progress means our registry holds nothing graded on this question. The label describes the reach of our catalogue rather than the state of the science, and it counts as a finding neither for nor against.

Why it matters. On this site it carries a dashed chip, as No primary evidence does, because an absence sits off the ladder. A question nobody has graded must never look like one graded Low.

Related: No primary evidence vs Not-supported · evidence grade ladder

The CB1 receptor (cannabinoid receptor type 1) is the cannabinoid receptor behind intoxication: THC activating it produces the "high." One of the two main cannabinoid receptors, it is dense throughout the brain and nervous system and normally answers to the endocannabinoids anandamide and 2-AG.

Why it matters: CB1 is where the line between intoxicating and non-intoxicating cannabinoids gets drawn. THC activates it as a partial agonist. In laboratory studies CBG blocks it (a CB1 competitive antagonist; Cascio 2010; Demonstrated · in vitro), which fits with CBG being non-intoxicating.

Related: CB2 receptor, Cannabinoid receptor, Endocannabinoid system (ECS), agonist, antagonist

The CB2 receptor (cannabinoid receptor type 2) is the second main cannabinoid receptor, found mostly outside the brain, especially on immune cells and in peripheral tissues. Activating it is generally unconnected with intoxication.

Why it matters: Its post in the immune system makes CB2 a favourite focus of preclinical inflammation research. Location tells researchers where to look. A benefit in people has to be shown separately.

Related: CB1 receptor, Cannabinoid receptor, Endocannabinoid system (ECS), endocannabinoid

CBGA (cannabigerolic acid, C₂₂H₃₂O₄, ≈ 360.5 g/mol) is the acidic precursor from which the plant builds the other major cannabinoid acids, often called the "mother acid." Synthase enzymes convert it into THCA, CBDA and CBCA, and CBGA itself decarboxylates to CBG. Established (chemical identity + biosynthetic role). Verified effect pharmacology for CBGA is minimal (catalogue in progress). Widely circulated claims, such as an in-vitro report that CBGA can bind a viral protein, are laboratory observations and not evidence that CBGA prevents or treats any disease in people.

Why it matters. Every branch of the family tree starts at CBGA, which is where CBG's "mother cannabinoid" name comes from and why this Atlas is built around it. The chemistry is settled. What CBGA does in people is not established, and any claim about it should stop where the chemistry does.

Related: biosynthesis · synthase enzyme · cannabinoid acid · decarboxylation

A Certificate of Analysis (COA) is the lab report that states what a product actually contains, ideally issued by an independent third-party laboratory. It reports the measured cannabinoid content (does it match the label?), the THC level (which bears on legality and drug testing), and screening for contaminants: pesticides, residual solvents, heavy metals and microbes. Established

Why it matters. Of everything a buyer can hold in their hand, the COA says the most about a cannabinoid product. A current, independent COA that matches the label lets identity and purity be checked instead of taken on trust; one that is missing, out of date or mismatched is a red flag.

Related: molecular formula · solubility · novel food status

In a crossover trial every participant receives both the intervention and the control, one after the other and usually with a washout period in between, so each person acts as their own comparison. The one human CBG trial in our registry (Cuttler 2024) and the CBN sleep-laboratory trial (Lavender 2026) both used a placebo-controlled crossover design. Established

Why it matters. The design needs fewer participants to detect a difference, at a price: it can test only short-lived, reversible effects. A single-dose crossover is silent on what months of daily use would do.

Related: randomized controlled trial (RCT) · placebo-controlled trial · primary endpoint

The cytochrome P450 (CYP450) enzymes are a family of mostly liver enzymes that metabolize (break down) most medicines and many other compounds. Some cannabinoids, CBD most prominently, have been reported in laboratory and early human studies to inhibit certain CYP450 enzymes. In principle that could slow the clearance of drugs taken alongside them and raise their levels. The effect is under active investigation and has not been fully characterized or quantified, which is why researchers flag a potential for cannabinoid–drug interactions. Emerging (reported, not established for any specific drug pairing — not medical advice; anyone taking medication should consult a clinician or pharmacist).

Why it matters. Behind the standard warning that cannabinoids may interact with medications sits this enzyme family. The sensible response is a conversation with a professional; the warning is not a prediction that any particular interaction will or won't occur.

Related: first-pass metabolism · bioavailability · preclinical vs clinical · evidence grade ladder

Decarboxylation is a reaction in which a molecule gives up a carboxyl group as carbon dioxide (CO₂). In cannabinoids, heat drives off that CO₂ and converts each acid to its neutral form: CBGA → CBG, THCA → THC, CBDA → CBD, CBDVA → CBDV. Conversion starts roughly above 100 °C and is commonly reported in about the 110–130 °C range, with CBDVA → CBDV reported at around 130 °C over ~30 minutes. Hotter conditions convert faster but risk degradation. Demonstrated (thermal chemistry; a fact of heating, not an effect claim).

Why it matters. One reaction separates raw cannabis (acids, non-intoxicating) from heated or aged cannabis (neutral, active forms). It happens in smoking, vaping, baking and lab sample prep, and it explains why a "raw" product behaves differently from a heated one. For an extractor or formulator, time and temperature decide how much of the acid has converted.

Related: cannabinoid acid · CBGA (cannabigerolic acid) · biosynthesis · varin cannabinoid

Δ⁹-THC (delta-9-tetrahydrocannabinol) is the main intoxicating cannabinoid, producing the cannabis "high" by activating the CB₁ receptor. The plant makes it as THCA, which heat converts into Δ⁹-THC. Established

Why it matters. US law defines hemp by Δ⁹-THC content, and standard drug tests look for its metabolite, THC-COOH. So a product's Δ⁹-THC, plus any THCA that heat will convert, decides both how it reads legally and how much drug-test risk it carries.

Related: CB1 receptor · total THC · THC-COOH · hemp (US legal definition) · decarboxylation

Desensitization is the loss of responsiveness in a receptor or ion channel after strong or repeated activation: the signal fades while the trigger is still present. Cells use it to protect themselves from over-stimulation, which means a single compound can first activate a target and then leave it desensitized.

Why it matters: That two-step explains how the same molecule can be called both an activator and a silencer of the same channels. In laboratory studies CBG activates the TRPV1 and TRPV2 channels and then desensitizes them (De Petrocellis 2011; Demonstrated · in vitro). Both labels are right. They describe different moments.

Related: trpv1, trpv2, agonist, CBG

An endocannabinoid is a cannabinoid the body makes itself (endo- means "within"). The main ones, anandamide and 2-AG, are signalling lipids produced on demand, active briefly at cannabinoid and related receptors, and then broken down by enzymes: the endocannabinoid system's own messengers.

Why it matters: Every plant cannabinoid gets measured against them, since it acts, often less precisely, on machinery the body built for these native molecules.

Related: anandamide, 2-AG (2-arachidonoylglycerol), Endocannabinoid system (ECS), Endogenous vs exogenous

The endocannabinoid system (ECS) is the body's cannabinoid signalling network: the cannabinoid receptors (chiefly CB1 and CB2), the endocannabinoids that activate them (such as anandamide and 2-AG), and the enzymes that make and break those molecules down. It runs through the brain, nervous system and peripheral tissues, fine-tuning many physiological processes and generally working to keep other systems in balance.

Why it matters: Plant-made, endogenous or synthetic, every cannabinoid ends up acting through the ECS, which makes it the foundation of the whole science. Its reach also explains why cannabinoid effects are rarely simple or narrowly targeted.

Related: CB1 receptor, CB2 receptor, endocannabinoid, anandamide, 2-AG (2-arachidonoylglycerol), Cannabinoid receptor

Endogenous means made inside the body; exogenous means coming from outside it. Anandamide and 2-AG are endogenous. Plant cannabinoids (phytocannabinoids such as CBG, CBD and THC) and lab-made cannabinoids are exogenous. Both kinds can act on the same receptors, but the body keeps a far tighter hand on its own: where they are made, when, and in what amount.

Why it matters: An exogenous cannabinoid slips that control. Once it arrives from a gummy or an oil, its dose, timing and breakdown are out of the hands of the body's own signalling.

Related: endocannabinoid, phytocannabinoid, Endocannabinoid system (ECS)

The entourage effect is the idea that the compounds in cannabis act differently, or better, together than a single purified cannabinoid does alone. Its support is mostly preclinical or theoretical. Controlled human trials showing whole-plant blends outperforming matched isolates are lacking, so it remains an unproven hypothesis. Hypothesized

Why it matters. Every "full-spectrum works better" label leans on this idea. The evidence grades it a hypothesis, so a claim built on it says more than the research shows.

Related: full-spectrum, broad-spectrum and isolate · cannabinoid · evidence grade ladder

The evidence grade ladder is the six-rung scale CBG Atlas uses to rate how strongly the evidence supports a specific claim. From strongest to weakest the rungs are Established › Demonstrated › Emerging › Low › Hypothesized › Not-supported. Each substantive claim on the platform gets one, and the type and amount of evidence behind the claim set the rung:

- Established: ≥2 independent human randomized controlled trials (RCTs) show the effect. The top rung, and the most reliable. - Demonstrated: ≥1 robust human RCT, or ≥2 human observational studies. Strong, one step short of independent RCT replication. - Emerging: early human data (≥1 human study, which may be a small or acute RCT), or ≥2 independent animal studies that agree (a "convergent preclinical signal"). - Low: one effect study that falls short of Emerging, for instance a single animal study or in-vitro work alone. - Hypothesized: evidence that is only mechanistic, such as a receptor-binding study, with nothing that measured an effect. The mechanism is plausible; the effect is undemonstrated. (Cascio 2010, a receptor-binding study, is an example: it establishes a mechanism and stops short of a clinical effect.) - Not-supported: the claim was tested, and the evidence went against it. That makes it a finding against the claim, and the rarest rung, since it needs real contradicting data.

Not a rung: No primary evidence. When no primary study exists because nobody has done the experiment, the label is No primary evidence / catalogue in progress, a coverage state that sits off the ladder. Recording it as Not-supported would claim a negative finding we do not have, so it never is.

Established: the ladder itself is the platform's own defined editorial standard.

Why it matters. A grade travels with the fact. A reader, or an AI quoting the page, takes away how strong the evidence is along with the claim, and "we don't know yet" becomes a visible, respectable answer instead of a gap to paper over.

Related: in vitro vs in vivo · preclinical vs clinical · randomized controlled trial (RCT) · Certificate of Analysis (COA)

First-pass metabolism (the "first-pass effect") is the partial breakdown of a swallowed substance by the gut and liver before it reaches the general bloodstream. Swallowed cannabinoids undergo a substantial first-pass effect, one reason their oral bioavailability is generally low, and routes that partly bypass the liver (such as sublingual or inhaled) behave differently. Established

Why it matters. Together with poor solubility, it explains why the amount on a label is not the amount that reaches the bloodstream, and why changing the route of administration reshapes the whole picture. A capsule and a sublingual oil can carry the same milligram count and still deliver different amounts.

Related: bioavailability · CYP450 enzymes · solubility

These three terms describe how much of the plant's chemistry a hemp product keeps. Full-spectrum retains the naturally occurring cannabinoids and terpenes, trace THC included (≤0.3% Δ⁹-THC in US hemp). Broad-spectrum keeps multiple compounds with the THC stripped out. Isolate is one purified cannabinoid and nothing more. Established

Why it matters. The three words describe composition and stay silent on efficacy. Where they do speak is drug-test risk, because the trace THC in full-spectrum products can accumulate.

Related: entourage effect · certificate of analysis (COA) · THC-COOH

In US federal law, hemp is cannabis with at most 0.3% Δ⁹-THC by dry weight, a definition in place since the 2018 Farm Bill; cannabinoids derived from hemp are generally read as sharing its status. Many states and enforcement positions measure total THC instead, which counts THCA. General information, not legal advice. Established

Why it matters. A product's legal status can turn on which THC figure is used. THCA-rich flower is the standard example: legal under one reading, out of bounds under the other.

Related: total THC · cannabinoid acid · novel food status

Homologs are relatives in a chemical series that differ from one another by a repeating unit. In cannabinoids that unit sits in the side chain: THCV, CBDV and CBGV are the three-carbon (propyl) homologs of THC, CBD and CBG. Established

Why it matters. Changing the side chain produces a new molecule with its own pharmacology. THCV does not act like THC, and each homolog has to earn its evidence apart from its parent.

Related: varin cannabinoid · pentyl vs propyl side chain · isomer

An immunoassay is the standard screening test for cannabis use, using antibodies to detect THC's main metabolite, THC-COOH. Related molecules can cross-react with some immunoassays. CBN is one of them, which is part of why CBN products carry a drug-test risk. Established

Why it matters. A screen reacts to a class of molecules, whatever the label says. "Non-intoxicating" and "test-safe" are separate claims, and a product can meet the first and fail the second.

Related: THC-COOH · full-spectrum, broad-spectrum and isolate

In vitro ("in glass") means tested outside a living organism, in cells, tissues or isolated proteins; in vivo ("in the living") means tested inside one, whether an animal or a person. A large share of cannabinoid pharmacology is in vitro. De Petrocellis 2011, for example, characterized cannabinoid activity at TRP ion channels in isolated systems (in vitro), whereas Borrelli 2013 tested CBG in a mouse model of colitis (in vivo, animal). Established (definitional distinction).

Why it matters. A result in a dish shows what a molecule can do to cells. What it does in a person is a separate question with a separate answer, and the grade ladder keeps the two apart for exactly that reason.

Related: preclinical vs clinical · evidence grade ladder · randomized controlled trial (RCT)

"Intoxicating" means causing impairment or a "high," as THC does; "psychoactive" is the wider term for anything that affects the brain. A compound can be psychoactive without being intoxicating, which makes the two words far from interchangeable. Established

Why it matters. CBG, CBD, CBC and CBDV are non-intoxicating. Whether they have subtler effects on mood is a separate question, and for most of them it is not established. On a label, "non-intoxicating" is the accurate word; "non-psychoactive" claims more than the evidence shows.

Related: CB1 receptor · partial agonist

An inverse agonist binds the same receptor an agonist would but pushes its activity below the normal resting (baseline) level. A plain antagonist stops at blocking activation; the inverse agonist goes further and drives activity down. The difference exists only at receptors that show some activity of their own when unstimulated.

Why it matters: Blocking a signal and suppressing it below baseline are different actions, and cannabinoid reporting mixes them up often.

Related: agonist, antagonist, Partial agonist, Cannabinoid receptor

Isomers are molecules that share a molecular formula but arrange their atoms differently, which can change their properties. CBD and THC are the standard cannabinoid example: both are C₂₁H₃₀O₂, yet one has an open ring and the other a closed ring, and their effects differ. Δ⁹-THC and Δ⁸-THC are isomers too, differing only in where a single double bond sits. Established

Why it matters. Sharing a formula makes two molecules neither identical nor alike in effect. Close cannabinoid relatives can behave very differently, and Δ⁸ versus Δ⁹ on a product is a real chemical difference.

Related: molecular formula · molar mass (molecular weight) · pentyl vs propyl side chain

logP measures lipophilicity, a compound's preference for oil or fat over water; formally, it is the base-10 log of the compound's oil-to-water partition ratio. The higher the value, the more fat-loving and water-avoiding the molecule. Cannabinoid values are high, with CBD and THC reported around 6–7, which is why they dissolve easily in oils, fats and ethanol and hardly at all in water. For many minor cannabinoids and acids the figure is not established (catalogue in progress). Established (a physicochemical constant, not a potency value).

Why it matters. This one number explains most of how a cannabinoid behaves in a product: why it is sold as an oil, tincture or emulsion, why absorption is erratic, and why stirring it into water fails.

Related: solubility · bioavailability · first-pass metabolism · molecular formula

A minor cannabinoid is any cannabinoid the plant produces in small quantities, which in practice means anything other than THC and CBD, the two most abundant. CBG is central to the group, since its acid, CBGA, is the precursor the plant turns into the rest. Established

Why it matters. What these molecules are is settled. What they do in people mostly is not: human evidence for most of them is thin or absent, a catalogue in progress. The name on a label identifies a molecule, and any effect has to be shown separately.

Related: cannabinoid · CBGA · varin cannabinoid · catalogue in progress

Molar mass, also called molecular weight, is the mass in grams of one mole of a substance (g/mol), found by summing the masses of all the atoms in its molecular formula. CBG (C₂₁H₃₂O₂) comes to about 316.5 g/mol and its acid, CBGA (C₂₂H₃₂O₄), to about 360.5 g/mol. Established

Why it matters. Chemists use molar mass to convert between mass and number of molecules. The ≈ 44 g/mol gap between an acid and its neutral form is the mass of the CO₂ lost during decarboxylation, the same loss that total-THC calculations correct for with the 0.877 factor.

Related: molecular formula · decarboxylation · cannabinoid acid

A molecular formula counts the atoms of each element in a molecule. Cannabinoid formulas almost always contain only carbon (C), hydrogen (H) and oxygen (O): CBG is C₂₁H₃₂O₂ (21 carbons, 32 hydrogens, 2 oxygens), and its acid CBGA is C₂₂H₃₂O₄. Established

Why it matters. The formula is the first identity check, the entry a COA or a reference database such as PubChem or CAS starts from. Pinning down which molecule you actually have takes more, because isomers share a formula.

Related: isomer · molar mass (molecular weight) · Certificate of Analysis (COA) · cannabinoid acid

No primary evidence and Not-supported sound alike and mean very different things, and this platform keeps them apart. No primary evidence means our registry holds no study of the question in either direction. Not-supported means the question was tested and the evidence went against the claim.

Why it matters. Take two CBG questions. Eye pressure has no primary evidence. Sleep was tested in a placebo-controlled trial and came out Not-supported. File the sleep result alongside the eye-pressure gap and a real finding disappears.

Related: evidence grade ladder · primary endpoint

A novel food, in EU and UK regulation, is a food with no significant history of consumption before May 1997, and it can be sold as a food or supplement only once it has been authorized for safety. As of 2026-07-12, EU and UK authorities broadly class extracted cannabinoids such as CBD and CBG as novel foods that require authorization, and many cannabinoid products are pending or unauthorized. Canada takes a different route, regulating phytocannabinoids under the Cannabis Act rather than as foods. Status changes over time, so treat this as dated, general information — not legal advice and check it against official sources. Established (regulatory status as dated; a legal category, not a safety verdict).

Why it matters. The same CBG oil can be on open sale in one jurisdiction and unauthorized in the next. Anyone selling across borders has to check the status market by market, and read it with a date.

Related: Certificate of Analysis (COA) · cannabinoid

A partial agonist activates a receptor but produces only a submaximal response, even when it occupies every available receptor. Set beside an empty receptor it looks activating; set beside a full agonist it can look dampening. THC is the textbook partial agonist at the CB1 receptor.

Why it matters: That partial activity at CB1 shapes THC's intoxicating effect, and helps explain why dose and context matter so much with cannabinoids.

Related: agonist, antagonist, Inverse agonist, CB1 receptor

Pentyl and propyl name the two side-chain lengths found in cannabinoids: five carbons and three. The side chain is the hydrocarbon "tail" (an alkyl chain) on the ring system. CBG, CBD and THC carry the five-carbon pentyl chain; the varin cannabinoids carry the three-carbon propyl chain, shorter by two CH₂ units. So CBG (C₂₁H₃₂O₂, pentyl) pairs with CBGV (C₁₉H₂₈O₂, propyl). Established

Why it matters. Two carbons are the whole difference between the familiar cannabinoids and the varin branch, and they are enough to make each varin a compound in its own right: CBGV, THCV and CBDV are separate compounds from CBG, THC and CBD, not other names for them.

Related: varin cannabinoid · isomer · molecular formula · biosynthesis

Pharmacokinetics (PK) describes what the body does to a compound over time: absorption, distribution, breakdown and elimination. PK is the science behind onset, duration, and how long a substance remains detectable. Established

Why it matters. Human PK data for most minor cannabinoids are thin or unpublished, and for CBN they are unpublished. Sound timing or dosing guidance depends on those data, which is why the Atlas stays out of dosing.

Related: bioavailability · first-pass metabolism · CYP450 enzymes

A phytocannabinoid is a cannabinoid made by the cannabis plant (phyto- means "plant"). CBG, CBD, THC, CBC, CBN and their acid forms all qualify. They are exogenous, and they interact, with varying selectivity, with the endocannabinoid system and a range of other targets.

Why it matters: The label is handy and it misleads, because it implies a shared pharmacology these compounds lack. In laboratory studies CBG and THC push the CB1 receptor in opposite directions.

Related: endocannabinoid, Endogenous vs exogenous, Cannabinoid receptor, CBG

A phytocannabinoid is a cannabinoid made by a plant (phyto- = plant): CBG, CBD, THC and the rest of the cannabis cannabinoids. An endocannabinoid is one made inside the body (endo- = within), a signalling molecule such as anandamide or 2-AG that acts on the body's own cannabinoid receptors. Both act on the endocannabinoid system; one starts in the plant, the other in human physiology. Established

Why it matters. The body already runs a cannabinoid-signalling system of its own, and plant cannabinoids are outside molecules interacting with it. Keeping that straight helps explain mechanism without overstating it.

Related: cannabinoid · cannabinoid acid

A placebo-controlled trial is a study in which the comparison group receives an inactive look-alike, so a real effect can be told apart from expectation and chance. If the trial is double-blind, neither the participants nor the researchers know who got what. Established

Why it matters. People often feel better simply because they are being treated. A placebo arm is what lets an improvement be credited to the compound.

Related: randomized controlled trial (RCT) · crossover trial · primary endpoint

Preclinical research comes before any human testing and uses cells (in vitro) or animals (in vivo); Borrelli 2013, which studied CBG in mouse colitis, is preclinical. Clinical research is carried out in people, in human trials. A promising preclinical finding earns further investigation, and only clinical research can show that something works in humans. Established (definitional distinction).

Why it matters. Most cannabinoid evidence today is preclinical. Labelling it that way keeps early hints from passing as human proof, and the grade ladder is built to make the gap visible.

Related: in vitro vs in vivo · randomized controlled trial (RCT) · evidence grade ladder

A trial's primary endpoint is the one outcome it commits to in advance as its main test: the result the study was built to detect. Other outcomes it measures rank below it as secondary or tertiary endpoints. Established

Why it matters. Missing the primary endpoint means the trial did not show what it set out to show, however much a secondary outcome moved. CBN and sleep is graded Not-supported for exactly this reason: both CBN sleep trials that named a primary endpoint in advance missed it (Bonn-Miller 2024; Lavender 2026).

Related: randomized controlled trial (RCT) · no primary evidence vs Not-supported · placebo-controlled trial

A randomized controlled trial (RCT) is a human study in which chance decides who receives the intervention and who receives a control, often a placebo. Random assignment makes the groups comparable, so a difference in outcomes can be put down to the intervention rather than to chance or bias. Well-conducted RCTs, independently replicated, are the strongest evidence of whether something works in people. Established (definitional; the methodological gold standard).

Why it matters. The top of the grade ladder rests on RCTs: "Established" requires independent human ones. An RCT is what moves a claim from "looks promising in a dish or an animal" to "shown to work in people."

Related: evidence grade ladder · preclinical vs clinical · in vitro vs in vivo

Receptor affinity is how tightly a molecule binds a receptor. A high-affinity compound occupies the receptor at low concentrations; a low-affinity one needs more to fill the same receptors. Affinity describes binding only. Efficacy, what the receptor does once bound, is a separate property, and a binding measurement by itself is silent on effects in a person.

Why it matters: Few numbers in cannabinoid science are misread more often, because a strong binding value looks like a benefit. So the actual affinity and potency values (the specific binding constants) stay on our researcher-tier pages, and we do not show them here.

Related: agonist, Partial agonist, Cannabinoid receptor, how we grade evidence

Solubility is the amount of a substance a given liquid can dissolve. Being lipophilic (fat-loving), cannabinoids are practically insoluble in water while dissolving freely in oils, fats and organic solvents like ethanol. CBD, for scale, dissolves in water on the order of ~12.6 mg/L, a vanishingly small amount. Established

Why it matters. Hence the oils, ethanol tinctures and specially engineered emulsions on the shelf, and a major reason absorption is low and variable. High logP is the cause; poor water solubility is the problem a formulator has to work around.

Related: logP / lipophilicity · bioavailability · first-pass metabolism

A synthase is an enzyme that makes one specific product. Cannabis has three branch-point synthases, THCA synthase, CBDA synthase and CBCA synthase, and each turns the shared precursor CBGA into a different acid: THCA, CBDA or CBCA. The set a plant expresses largely fixes its chemotype, whether THC-rich, CBD-rich or otherwise. Established (The parallel varin-branch synthases are less fully characterized: catalogue in progress.)

Why it matters. These enzymes are the switches between one mother acid and the plant's many cannabinoids. They account for the shape of the family tree, and for why one cultivar runs high in THC and another high in CBD.

Related: biosynthesis · CBGA (cannabigerolic acid) · cannabinoid acid · varin cannabinoid

THC-COOH is THC's main metabolite, and the molecule standard cannabis drug tests are built to detect. Established

Why it matters. Anything that delivers THC can generate THC-COOH and a positive result. That includes full-spectrum products with trace THC, and THCA once it has been heated.

Related: immunoassay drug screen · total THC · decarboxylation

Total THC is an estimate of how much THC a product will deliver after heating, calculated as Δ⁹-THC plus 0.877 × THCA. The 0.877 factor accounts for the carbon dioxide THCA loses as it converts. Established

Why it matters. Under a Δ⁹-only test, THCA-rich flower can read as hemp; under total THC it usually reads as something else. Which standard applies varies by jurisdiction, so the THC line on a COA has to be read against the local rule.

Related: decarboxylation · hemp (US legal definition) · cannabinoid acid

TRPA1 is a TRP ion channel, one of the family of molecular sensors that also includes TRPV1, TRPV2 and TRPM8, and like its relatives it sits outside the classic CB1/CB2 cannabinoid system.

Why it matters: For CBN and CBC, verified targets are scarce, and TRPA1 is one of the few. In laboratory studies CBN acts on TRPA1 as a potent agonist and desensitiser, and CBC also acts on it (De Petrocellis 2011; Demonstrated · in vitro).

Related: trpv1, trpm8, agonist, desensitization

TRPM8 is the ion channel that senses cold and menthol; activating it produces menthol's cooling sensation. A gated pore in the cell membrane, it is one of several TRP channels some cannabinoids engage, and a compound can either activate it or block it.

Why it matters: The cold sensor is one more place where CBG's pharmacology turns up far from CB1 and CB2. In laboratory studies CBG acts as a TRPM8 antagonist (De Petrocellis 2011; Demonstrated · in vitro).

Related: trpv1, trpv2, antagonist, CBG

TRPV1 is the heat-sensing ion channel that capsaicin, the source of a chilli pepper's burn, activates. A TRP channel involved in pain and temperature signalling, it is among the targets beyond CB1/CB2 that several cannabinoids engage. Strong activation switches it on and then leaves it desensitized.

Why it matters: CBG runs through both stages here. In laboratory studies CBG acts as an agonist-then-desensitizer at TRPV1 (De Petrocellis 2011; Demonstrated · in vitro): it first activates the channel, then leaves it less responsive.

Related: trpv2, trpm8, desensitization, CBG

TRPV2 is a heat- and stretch-sensitive ion channel, a close relative of TRPV1 involved in sensory and other signalling. It is another TRP channel outside the classic cannabinoid receptors that some cannabinoids act on, and like its cousin it can be activated and then desensitized.

Why it matters: CBG repeats the TRPV1 pattern here. In laboratory studies CBG is an agonist-then-desensitizer at TRPV2 as well (De Petrocellis 2011; Demonstrated · in vitro), part of the broad panel of targets that sets its pharmacology apart.

Related: trpv1, trpm8, desensitization, CBG

Varins are the propyl series of cannabinoids, carrying a three-carbon side chain: CBGV, THCV, CBDV, the shorter-chain homologues of CBG, THC and CBD. The plant builds them from their own "mother acid," CBGVA (cannabigerovarinic acid), in a branch that runs parallel to the pentyl CBGA pathway. Each is a distinct molecule from its pentyl parent; CBGV is C₁₉H₂₈O₂, where CBG is C₂₁H₃₂O₂. Their identities are well established, while much of their pharmacology is still catalogue in progress. Established (for identity and biosynthetic relationship).

Why it matters. Names this close to the familiar cannabinoids invite mix-ups on a label or a search page. THCV is not THC; CBDV is not CBD. Chemistry is what separates them.

Related: pentyl vs propyl side chain · cannabinoid acid · biosynthesis · CBGA (cannabigerolic acid)